Plasmopara viticola. [Descriptions of Fungi and Bacteria].

Author(s):  
G. Hall

Abstract A description is provided for Plasmopara viticola. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Ampelopsis brevipedunculata, A. hederacea, A. heterophylla, A. veitchii, Ampelocissus acetosa, A. latifolia, A. salmonea, Cissus caesia, C. gracilis, C. hypoglauca, C. polyantha, Cordifolia sempervirens, Cinerea sp., Parthenocissus quinquefolia, P. tricuspidata, Solonis robusta, Vitis aestivalis, V. amurensis, V. arizonica, V. berlandieri, V. californica, V. cinerea, V. coignetiae, V. cordifolia, V. girdiana, V. labrusca, V. lanata, V. monticola, V. pagnuccii, V. riparia, V. romaneti, V. rupestris, V. silvestris, V. treleasei, V. vinifera. DISEASE: Grape vine downy mildew; the fungus is an obligately biotrophic plant pathogen. All tissues bearing stomata are infected, becoming discolored, malformed and necrotic. Lesions on affected organs develop a white felt of sporangiophores. Leaves are most susceptible to attack during active growth in early summer, and when very mature in the autumn. Sporangiophores may appear directly on healthy green leaf tissues with no overlying lesion, or as a dense felt under yellow oily lesions on the upper surface (if humidity is high, 5-15 days after infection), or may be absent, leaves presenting only a mosaic of small, angular yellow or dark-red blemishes, limited by the secondary veins (mainly on old leaves in the autumn). During early growth, whole branches are attacked, but later only the extremities of branches are invaded. Infected shoots turn brown, curl up or become hooked at their tips. Nodes are more susceptible to attack than internodes. Tendrils, petioles, inflorescences and bunches also develop similar brown spots and lesions. Bunches are susceptible until the grapes are 5-6 mm diam., after which infection is rare (grey rot followed later by brown rot). Subsequent browning and desiccation of the bunch is caused by penetration of the bunch stalk by mycelium from earlier infections elsewhere. GEOGRAPHICAL DISTRIBUTION: See CMI Distribution Maps of Plant Diseases 221. TRANSMISSION: Oospores present in infected leaf tissues from the previous season's crop germinate in the spring, when air temperatures exceed 12°C and at least 10 mm rain falls in 24 hours, releasing zoospores into water or onto very moist soil from sporangia (64, 2458). Zoospores are projected onto vine leaves near the soil by rain splash, germinate to give hyphae and penetrate tissues via their stomata. Sporangia are liberated in moist air only, are disseminated by air currents, and remain viable for five days in dry air, producing secondary infection sites. Production of sporangia occurs at a relative humidity of 95-100%, and an air temperature of 13-27°C (optimum 18-22°C). Mycelium may overwinter between the bud scales and in diseased leaves, but it has not been established whether this contributes substantially to re-infection of healthy leaf tissues the following spring. There is no evidence for systemic transmission.

Author(s):  
G. Hall

Abstract A description is provided for Plasmopara halstedii. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Over 80 hosts from a wide range of genera in the Compositae have been reported, including wild and cultivated species of Helianthus. For lists see Leppik (1966) and Novotel'nova (1977). DISEASE: Downy mildew of sunflower (Helianthus annuus var. macrocarpus); the fungus is an obligately biotrophic plant pathogen. Leaves of infected plants develop chlorotic mottling which spreads from the veins near the petiole across the lamina, and increases in area and intensity as leaves age. Plants become stunted, having thin stems, very much smaller capitula without seeds, and smaller and darker roots. The disease is primarily systemic and mycelium can be found throughout the plant from roots to capitulum and achenes, in all except meristematic tissues. Under humid conditions, a white felt of sporangiophores develops on the undersurface of chlorotic areas. Localized secondary infection of the leaves and heads occasionally develops, resulting in spots, delimited by veins. Such secondary infection may also become systemic. Some infected plants show no disease symptoms, but produce lower yields of poorer quality seeds, which lose vitality and have lower germination rates (latent infection). Cotyledons are also infected causing damping-off in seed beds. A basal gall may also be produced. GEOGRAPHICAL DISTRIBUTION: Plasmopara halstedii is a fungus characteristic of the Americas, its putative origin, It has spread throughout Europe to parts of Africa and Asia, and has recently been reported from New Zealand. See CMI Distribution Maps of Plant Diseases 286. TRANSMISSION: Soil-borne oospores and mycelium (in systemically infected roots) overwinter, infecting subsequent crops. Sporangia form on the surface of infected seedling roots, releasing zoospores which encyst and germinate c root hairs of other seedlings, producing a systemic infection. Sporangia are dispersed by rain-splash from leaves, producing a secondary infection in plants up to the six-leaf stage, but infect only the apical growing points of olde plants. Transmission by oospores in seeds has been responsible for the spread of this fungus around the world, especially since these spores can germinate to produce only a latent infection in the host plant (53, 4545).


Author(s):  
J. C. David

Abstract A description is provided for Passalora sojina. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. DISEASE: Frog-eye leafspot. HOSTS: Glycine hispida, G. javanica, G. max, G. soja, G. ussuriensis (FALEEVA, 1976), Mucuna sp. (CROUS & BRAUN, 2003) (Fabaceae). GEOGRAPHICAL DISTRIBUTION: [CAB International Distribution Maps of Plant Diseases No. 871, Edn. 1 (2002)]. AFRICA: Cameroon, Côte d'Ivoire, Egypt, Gabon, Kenya, Malawi, Nigeria, Zambia, Zimbabwe. NORTH AMERICA: Canada (Ontario), Mexico, USA (Alabama, Arkansas, Delaware, Florida, Georgia, Hawaii, Illinois, Indiana, Iowa, Kansas, Louisiana, Maryland, Michigan, Mississippi, Missouri, New Jersey, New York, North Carolina, Oklahoma, South Carolina, Texas, Virginia, West Virginia, Wisconsin). CENTRAL AMERICA: Cuba, Guatemala. SOUTH AMERICA: Argentina, Bolivia, Brazil (Goias, Maranhao, Mato Grosso, Minas Gerais, Parana, Pernambuco, Piaui, Rio Grande do Sul, Santa Catarina, Sao Paolo), Venezuela. ASIA: China (Fujian, Gansu, Guangxi, Hebei, Heilongjiang, Henan, Jiangsu, Jiangxi, Jilin, Liaoning, Nei Menggu, Sichuan, Yunnan, Zhejiang), East Timor, India (Karnataka, Meghalaya, Sikkim, Uttar Pradesh), Japan, Nepal, Russia (Far East), South Korea, Taiwan. EUROPE: Russia. TRANSMISSION: Seedborne and by aerial dispersal of conidia through wind and rain splash. The fungus also survives in dead plant material and can re-infect living plants (SWEETS, 2001).


Author(s):  
M. A. J. Williams

Abstract A description is provided for Sclerotinia narcissicola. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOST: Narcissus spp. DISEASE: Smoulder, grey mould. Infection may reduce bulb yield and flower size (55, 3617). Symptoms may include: rot of the bulbs and leaves at ground level, brown lesions on the leaves and flower buds, distortion and failure of emergence. GEOGRAPHICAL DISTRIBUTION: Asia: Iraq, USSR; Australasia: Australia (Tasmania, Victoria), New Zealand; Europe: Channel Islands (Guernsey, Jersey), Denmark, Eire, England, Germany, Northern Ireland, The Netherlands, Norway, Scotland, Sweden, USSR, Wales, West Germany; North America: Canada (British Columbia, NS, Ontario, PEI); USA (North Carolina, New York, Oregon, Virginia, Washington State) (see CMI Distribution Maps of Plant Diseases, No. 315). TRANSMISSION: The disease may come from planting of infected bulbs or from infected soil; sclerotia in the soil may be viable for up to nine months (61, 7053). In vitro conidial suspensions did not cause infection except of wounded or damaged tissue; mycelial inoculation consistently caused lesions on detached leaves and bulb scales (61, 5797).


Author(s):  
V. P. Hayova

Abstract A description is provided for Valsa sordida. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. DISEASE: Valsa sordida is usually associated with Valsa canker of poplar twigs. Wounded trees, and trees injured by insects or attacked by other pathogens are more susceptible to infection. Development of Valsa canker is affected by environmental stress (Guyon, 1996; Tao et al., 1984). Poplar canker caused by V. sordida has been studied in different countries (CMI Distribution Maps of Plant Diseases, 1977; Worrall, 1983; Wang et al., 1981) The fungus can be often found in declining poplar stands together with another pathogen of poplar trees, Leucostoma niveum. Valsa sordida may also cause necrosis of willow twigs. HOSTS: Populus spp., Salix spp. and, more rarely, other woody angiosperms. GEOGRAPHICAL DISTRIBUTION: Africa: Morocco. Asia: Armenia, Azerbaijan, China, Republic of Georgia, India, Iran, Iraq, Israel, Japan. Kazakhstan, Korea, Russia (Tatarstan), Turkey, Turkmenia, Uzbekistan. Australasia: Australia (Victoria), New Zealand. Europe: Austria, Belgium, Bulgaria, Czech Republic, Denmark, Estonia, France, Germany, Greece, Ireland, Italy, Netherlands, Norway, Poland, Portugal, Rumania, Russia, Slovakia, Sweden, Switzerland, UK, Ukraine, former Yugoslavia. North America: Canada (Alberta, British Columbia, Nova Scotia, Ontario, Québec, Saskatchewan). USA (California, Colorado, Michigan, Minnesota). South America: Chile. TRANSMISSION: Both conidia and ascospores are air-borne, especially under humid conditions. Yellow or orange exudation of conidia from conidiomata can be often seen after rain.


Author(s):  
J. M. Pérez

Abstract A description is provided for Sporisorium sorghi. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. DISEASE: Covered smut or covered kernel smut of sorghum. Development of functional ovaries and anthers is prevented in infected parts of the plants. HOSTS: Panicum miliaceum, Sorghum bicolor, S. dochna, S. halepense, S. plumosum, S. sudanense and S. vulgare (Poaceae). This species has also been recorded from Ischaemum ciliare (VISWANATHAN et al., 2000). GEOGRAPHICAL DISTRIBUTION: Worldwide, see CMI Distribution Maps of Plant Diseases No. 220, edn 4 (1987). In addition it has been recorded from AFRICA: Mauritania (FRISON & SADIO, 1987). CENTRAL AMERICA: Nevis. TRANSMISSION: In addition to dissemination on infected seed, there is evidence that this species can also be spread by air-borne chlamydospores (SHENOI & RAMALINGAM, 1976).


Author(s):  
K. H. Anahosur

Abstract A description is provided for Ramulispora sorghicola. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On Sorghum bicolor, S. halepense, S. nitidum, S. vulgare, Sorghum spp. (wild). DISEASE: Leaf spot. Small water-soaked lesions develop into oval to elliptical spots up to 7 × 3 mm, delimited by veins, with dark red or tan border up to 1 mm wide. Spots become irregular by 2-3 spots coalescing, with pinkish grey to straw necrotic centres. A few black sclerotia are found on the lower surface of roots. GEOGRAPHICAL DISTRIBUTION: Africa (Ethiopia, Nigeria, Malawi, Upper Volta); Asia (India, Indonesia, Pakistan). TRANSMISSION: The fungus can survive in the fragments of infected leaf tissues which remain on the ground and produce masses of conidia in damp weather which are disseminated by rain and wind. Sclerotia also survive and produce conidia in damp weather (Harris, 1960; Tarr, 1962). Wild species of sorghum act as collateral hosts.


Plant Disease ◽  
2005 ◽  
Vol 89 (7) ◽  
pp. 777-777 ◽  
Author(s):  
B. X. Killigrew ◽  
K. Sivasithamparam ◽  
E. S. Scott

Grapevine downy mildew, caused by the obligate, oomycete pathogen, Plasmopara viticola, was first recorded in Western Australia (W.A.) in 1998 (2) and has subsequently been observed in most viticultural regions of the state. Heterothallism in P. viticola was established by Wong et al. (3), whereby more than one mating type of the pathogen is required for sexual reproduction to occur. Oospores are considered to be the source of primary inoculum for this disease with further, secondary infection being advanced by asexual inoculum. However, recent research in European vineyards suggests that the majority of infection throughout the growing season arises via sexually derived (oosporic) inoculum (1). Since downy mildew is relatively new to W.A., few surveys have been conducted to study populations of the pathogen within the state. It is also noteworthy that the incidence of oospores in Australian vineyards has not been reported. The objective of this research was to assess the occurrence and type of inoculum of P. viticola in W.A. vineyards. A total of 1,266 P. viticola-infected leaf discs (LD) from eight wine-grape (775 LD), five table-grape (450 LD), and seven unknown (41 LD) cultivars grown in 16 vineyards in 10 geographically separate regions of W.A. were collected in the growing seasons of 2001-2003. These regions range from Chittering in the north to Albany in the south and received 700 to 1,200 mm annual rainfall, mostly in winter. Each LD was cleared in 1 M KOH at 60°C for 12 to 24 h and then was assessed for the presence of oospores with light microscopy. Leaves showing “mosaic”-type lesions (older infection) late in the season were collected where possible to ensure colony maturity and an increased likelihood of oospore formation. All LD from all regions were negative for the presence of oospores except for samples from a single vineyard (approximately 1,200 mm annual rainfall), where all 140 LD from six wine-grape cultivars contained oospores. The discovery that oospores were present in only one of 16 sampled vineyards provides a rare opportunity to study gene flow in field populations of the pathogen with time and to determine sources of primary inoculum where overwintering of P. viticola may not involve oospores. References: (1) S. McKirdy et al. Plant Dis. 83:301, 1999. (2) A. Rumbou et al. Eur. J. Plant Pathol. 110:379, 2004. (3) F. P. Wong et al. Plant Pathol. 50:427, 2001.


Author(s):  
G. Hall

Abstract A description is provided for Peronospora rubi. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Rubus arcticus, R. caesius, R. canadensis, R. canescens, R. chamaemorus, R. cissiburiensis, R. cissoides, R. corylifolius egg. (R. caesius × tereticaulis, R. nemorosus), R. flagellaris, R. fruticosus egg. (R. bregutiensis, R. buschi, R. glandulosus, R. hirtus, R. menkei, R. seebergensis, R. tereticaulis, R. vulgaris), R. idaeus, R. laciniatus, R. leucodermis, R. × loganobaccus (orursinus × ideaus), R. occidentalis, R. parviflorus, R. plicatus, R. procerus, R. spectabilis, R. strigosus, R. sulcatus, R. tuberculatus, R. villosus, R. vitifolius, and certain hybrids, e.g. 'Tayberry' (blackberry cv. Aurora × tetraploid red raspberry), 'Tummelberry' (a 'Tayberry' interspecific cross) and 'Youngberry'. DISEASE: Downy mildew of cane fruits (Rubus spp.), especially blackberry (R. fruticosus agg.), boysenberry (a blackberry × red raspberry cross: the name R. × loganobaccus covers this plant) and raspberry (R. idaeus). The fungus, an obligately biotrophic plant pathogen, occurs on leaves in summer to autumn, producing small, conspicuous, irregularly shaped patches on upper leaf surfaces, starting near the petiole, then following leaf veins. Patches are initially yellow, becoming carmine-red, vinaceous or purple and are bordered by venation. The undersurface of the leaf shows only a pale area with a brownish edge, and brownish discoloration near and alongside veins. Sporophores are sometimes difficult to detect in the dense mat of leaf hairs, but are heaviest on lowest leaves, close to ground level, forming a buff-grey felt. In wild-growing European species of Rubus the fungus occurs exclusively on the leaves. In North America it attacks leaves of cultivated raspberry bushes, and in New Zealand the fruits, sepals and pedicels of boysenberry, causing the fruit to become dry and shrivelled (dryberry disease). Downy mildew has recently become a problem on certain berry cultivars in Eastern England (McKeown, 1988). GEOGRAPHICAL DISTRIBUTION: Africa: South Africa. Asia: USSR (Azerbaijan). Australasia & Oceania: New Zealand. Europe: Czechoslovakia, Denmark, Finland, France, Germany (GFR, GDR), Norway, Poland, Rumania, Sweden, Switzerland, United Kingdom, USSR (Latvia). North America: Canada (British Columbia), USA (IL, MD, OR, WA, WI). See CMI Distribution Maps of Plant Diseases 598. TRANSMISSION: Determined for boysenberry in New Zealand only (61, 4245), where it is a systemic disease confined to the outer cortex parenchyma, keeping pace with cell division at apical meristems. Systemic cane infection is often indicated by red streaking of stems and petioles linking successively diseased leaves on a shoot. Unfolding leaves are invaded during warm wet weather causing typical leaf symtoms. Stores produced on diseased shoots initiate secondary infections of flowers and developing berries. These berries then become an important source of inoculum for new cycles of the disease. They go largely unnoticed, since spores are partially hidden on the split berry surfaces or covered by the sepals. After harvest, infection of developing primocanes continues by internal mycelial growth and spore infection. Oospores form on root surfaces in dead cortex cells and leaves. Soilborne oospores may infect healthy plants established in former sites of infected root crowns.


Author(s):  
G. Hall

Abstract A description is provided for Aphanomyces cochlioides. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Amaranthus blitoides, A. retroflexus, Beta lomatogona, B. patellaris, B. patula, B. trigyna, B. vulgaris, B. vulgaris var. cicla, Celosia argentea, Chenopodium album, Dianthus chinensis, Echinocloa crus-gallii, Escholtzia californica, Gomphrena globosa, Kochia scoparia, K. scoparia var. culta, Lychnis alba, Mollugo verticillata, Papaver rhoeas, Portulaca oleracea, Salsola kali, Saponaria ocymoides, Spinacia oleracea, Tetragonia tetragonioides. DISEASE: Blackroot of sugar beet; the fungus is a facultatively necrotrophic plant pathogen. There is an early acute phase of short duration (causing pre-emergence and post-emergence damping off) and a later chronic phase which may persist throughout the life of the plant. Infection during seed germination is indicated by poor stands with killed seeds remaining in the soil to infect young seedlings emerging elsewhere. Seedling hypocotyls are infected at ground level, a water-soaked area extending up and down the hypocotyl or the upper part of the young taproot from the point of entry. The invaded root or hypocotyl rapidly becomes brownish and then assumes the characteristic jet black discoloration from which the disease derives its name. Soon after, the cortex of the hypocotyl dries, and the stem and hypocotyl shrink, leaving a thin strand of tissue. Oospores are easily seen in the collapsed root and hypocotyl tissue on microscopic examination. The chronic phase first appears on plants in late June to August. A greenish-yellow discoloration of the swollen hypocotyl develops, affected root tissues becoming dark brown, soft, water-soaked, splitting apart and eventually shrivelling. Plants are stunted and lower leaves turn yellow. GEOGRAPHICAL DISTRIBUTION: Asia: Japan. Australasia & Oceania: Australia (Qld). Europe: Austria, Denmark, England, France, Germany (GDR & GFR), Hungary, Ireland, Poland, Sweden, USSR (Russia). North America: Canada (Alberta, NS, Ontario, Quebec), USA (California, Connecticut, Indiana, Michigan, Maine, MT, North Dakota, Ohio, South Dakota, Texas, Washington State, Wisconsin). South America: Chile. See CMI Distribution Maps of Plant Diseases 596. TRANSMISSION: Presumably in soil by oospores originating from sloughed-off root tissues and germinating to produce zoospores. The conditions favouring oospore germination are however largely unknown. Survival may occur on alternative hosts present in the crop, so the disease may be difficult to eliminate. The disease is particularly severe in warm, wet conditions, less so in cool, wet weather.


Author(s):  
A. Sivanesan

Abstract A description is provided for Elsinoe veneta. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On Rubus spp., especially on European and American red raspberries (R. idaeus and R. idaeus var. oculentissimus), black raspberry (R. occidentalis) and on loganberries, boysenberries, youngberries, etc. (R. ursinus, R. villosus, R. vitifolius) and the European bramble (R. fruticosus). DISEASE: Cane spot or anthracnose of raspberry causing dwarfing of canes and often dieback from the tip. GEOGRAPHICAL DISTRIBUTION: Widespread, occurring especially in cooler temperate areas of North America, W. Europe and Australia (CMI Map 503, ed. 1, 1974). TRANSMISSION: Initially by wind-borne ascospores from overwintered fruiting bodies. Ascospore release usually continuing during spring-early summer (Burkholder; Jones) or until autumn (Harris; 37, 201). Also initially by rain-splashed conidia from mycelium in overwintered lesions (Burkholder; 6, 740; 42, 332). Secondary infection by conidia from current season's lesions. Role of perfect state uncertain in some areas (Burkholder; 42, 622; 43, 2354).


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